Thyroid Pharmacology Flashcards

1
Q

T/F iodide is the rate limiting step in thyroid hormon syntehsis

A

T

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2
Q

T/F more t4 than than t3 is produced by thyroid

A

T

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3
Q

T/F T4 and T3 are largely protein bound

A

T

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4
Q

T/F TSH is low in hypothyroidism

A

F

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5
Q

T4 half life

A

7 days –> longer than 1 day T3

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6
Q

Why is there high TSH/TRH in hypothyroidism?

A

body trying to compensate for low T3/T4

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7
Q

Goal of thyroid hormone replacement

A

not a cure, just replacement

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8
Q

Why is hypothyroidism treated with T4 vs T3

A

half life is longer, peripheral conversion of T4 to T3

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9
Q

Why do some people have persistence of symptoms after T4 tx?

A

small studies show no benefit of combo tx, might also depend on polymorphisms of type 2 deoiodinase gene

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10
Q

Indications for T3

A

thyroid cancer pts before radioactive iodine therapy and scans, myxedema coma

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11
Q

Side effects of levothyroxin

A

from inappropriate dosing, can also have coloring dye sensitivity

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12
Q

Starting dose of levothyroxin depends on:

A

age, degree of thyroid failure –> older or cardiac disease, use smaller doses

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13
Q

IV dose of levothyroxin

A

75% of oral dose

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14
Q

Target TSH on tx

A

6 weeks/half lives and TSH target of .5-5 (but best is .5-2.5

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15
Q

In which situation can TSH not be trusted?

A

secondary hypothyroidism –> need to check thyroid hormone levels

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16
Q

Why would TSH on tx be higher than expected?

A

noncompliance, drugs/conditions that decrease LT4 absorption, drugs that increase LT4 metabolism, increase TBG, progression of endogenous thyroid disease

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17
Q

Drugs that decrease LT4 absorption:

A

iron, calcium carbonate, aluminum hydroxide, sucralfate, colestipol, ppi –> can be an issue with maternal supplements

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18
Q

Conditions that decrease LT4 absoprtion:

A

small intestine disease,

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19
Q

Drugs that increase LT4 metabolism

A

phenocarbitol, carbamazepine, phenytoin, rifampin

20
Q

Causes of increase TBG

A

pregnancy, estrogens, hepatitis

21
Q

Why would TSH on tx be lower than expected?

A

dopamine, high dose glucocorticoids, decrease TBG, self administration of excess LT4, reactivation of Graves’ or development of nodules

22
Q

causes of decrease TBG

A

androgens, nephrotic syndrome, chronic liver disease, sever systemic illness

23
Q

Tx of myxedema coma

A

iv hydrocortisone, LT4 and LT3, tx of precipitating factors like infection

24
Q

Drug to avoid in myxedma coma

A

sedatives b/c of decrease drug metabolism

25
Q

Antithyroid drugs block:

A
  1. oxidation and iodination of Tg
  2. iodotyrosine coupling to form T3/T4

e.g. PTU, tapazole

26
Q

Indications of antithyroid drugs

A

Graves: cool down pt before RAI or surgery, adults who may achieve remission, children and adolescents

27
Q

Antithyroid drug of choice

A

methimazole –> longer half life than PTU –> both have latent period of improvement

28
Q

T/F methimazole is protein bound

A

F –> PTU is which is useful in tx of pregnant women in 1st trimester (can’t cross placenta)

29
Q

PTU increases/decreases T4 to T3 conversion

A

decreases

30
Q

Side effects of PTU

A

lupus, vasculitis, hepatitis –> more than methimazole

31
Q

T/F frequency of side effects of methimazole are dose related

A

T –> vs PTU which is pretty random

32
Q

Use methimazole in graves’ always except in:

A

1st trimester pregnancy, thyroid storm, adverse effects to methimazole

33
Q

Major side effects of antithyroid drugs

A

agranulocytosis, PTU hepatitis, MMI cholestasis, vasculitis, polyarthritis

34
Q

Tx of agranulocytosis

A

stop antitoyroid drug, broad spectrum ab, hospitalize if granulocyte<500

35
Q

Drugs that inhibit T4 to T3 conversion

A

PTU, glucocorticoids,propanolol

36
Q

Tx of thyrotoxicosis

A

beta blockers b/c not an issue of thyroid proliferation but simply higher release of thyroid hormone from cells –> atenolol or metoprolol

37
Q

Tx of subacute thyroiditis

A

NSAID

38
Q

Tx of thyroid storm

A

PTU/MMI, propanolol, hydrocortisone, SSKI drops

39
Q

Iodide uptake mediated by ___ in normal thyroid

A

Na+/I- symporter NIS

40
Q

Wolff-Chaikoff Effect

A

excess iodide transiently inhibits thyroid iodide organification –> in normal thyroid, gland can regulate this inhibitory effect // in individuals with underlying autoimmune disease, this suppressive effect may persist even after iodine levels normalize

41
Q

T/F wolff chiakoff can be beneficial in tx of graves

A

T –> persistent suppression can decrease thyroid hormone synthesis, supporting anti-thyroid tx

42
Q

Jod-Basedow effect

A

thyrotoxicosis produced by iodine exposure –> in nodules

43
Q

I131

A

emits gamma and beta particles for dx and tx –> dose dependent effect

44
Q

Contraindications of I131

A

breastfeeding/pregnant women, children

45
Q

T/F goal in graves is hypothyroidism

A

T

46
Q

Amiodoarone

A

anti-arrhythmia that is 37% iodine –> can cause hypo or hyperthyroidism
Type 1 hyperthyroidism: in pts with underlying thyroid nodular disease, increased thyroid hormone production –> iodine effect
Type 2 hyperthyroidism: in pts with normal thyroid –> destructive thyroiditis with increased thyroid hormone release –> direct toxic effect of amiodorone

47
Q

rTSH

A

used in thyroid cancer pts for dx and imaging –> avoids symptomatic hypothyroidism

TSH stimulates uptake of iodine //in pts with residual thyroid cancer, want to stimulate uptake of iodine as much as possible before doing scan –> normally let the pt go hypothyroid and then give iodine to measure effect –> now can give rTSH to avoid hypothyroid effects while still letting endogenous TSH to drop before the test